The tooth supporting tissues affected by periodontal disease include the gingival tissue (gums); periodontal ligament (connective tissue located between the cementum and alveolar bone); cementum (mineralized connective tissue covering the root surface of a tooth); and the alveolar bone (the bone socket). Depending on the progression of the disease, there may occur a destruction of the periodontal ligament (PDL), alveolar bone loss, and apical migration of the junctional epithelium. Advanced periodontal disease may result in the formation of periodontal pockets harboring bacterial plaque, loss of tooth supporting tissues and progressive loosening and eventual loss of teeth.
Current periodontal therapies are directed at arresting the progression of the pathological alterations due to periodontat disease, as well as promoting the repair or regeneration of the periodontal wounds. Such therapies include wound and bone regeneration using purified growth factors (See for example, Antonaides et al. U.S. Pat. Nos. 4,861,757, 5,019,559, and 5,124,316); using growth factors in combination with dexamethasone to enhance the mitogenic effect of the growth factor (Rutherford, U.S. Pat. No. 5,149,691); using root surface demineralization (Terranova et al., U.S. Pat. No. 4,702,734; for an excellent review see Lowenguth and Blieden, 1993, Periodontology 2000, 1:54-68); and the use of periodontal barriers such as membranes (Magnuson et al., U.S. Pat. No. 4,961,707), microparticles (Jernberg, U.S. Pat. Nos. 5,059,123 and 5,197,882), biodegradable polymers (Dunn et al., U.S. Pat. No. 5,077,049) and biocompatible porous material comprising expanded polytetrafluoroethylene (Scantlebury et al., U.S. Pat. No. 5,093,179).
Growth factors, particularly platelet-derived growth factors (PDGF) and insulin-like growth factor (IGF-1) are known to stimulate mitogenic, chemotactic and proliferative (differentiation) cellular responses. Root surface demineralization is known to enhance the binding of fibronectin and fibroblasts to the root surface. Periodontal barriers are used to exclude contact between the root surfaces and the gingival epithelium and connective tissue thereby creating a space to allow the entry of periodontal ligament (PDL) cells to colonize the root surfaces preferentially over gingival epithelial cells, gingival fibroblasts, or osteoblasts. Periodontal barriers have been designed so that they may also be used for the controlled delivery of chemotherapeutic agents such as tissue regenerative agents (i.e. growth factors), antibiotics, and anti-inflammatory agents to promote periodontal healing and regeneration.
Several major aberrations have been observed and recognized as the major causes for the failure of current periodontal regenerative therapies. These include downgrowth of the junctional epithelium, failure to etablish reattachment of newly formed PDL collagen fibers to the root surface, root resorption, ankylosis of the root to the surrounding alveolar process, and incomplete PDL regeneration. Ankylosis (See for example Antonaides et al., supra, and Magnuson et al., supra) occurs when periodontal regeneration does not occur in an orderly manner, i.e. bone cells reach the root surface where an imperfect and dysfunctional fusion occurs rather than bone cells being anchored to the root surface via a connective tissue attachment (cementum, and collagen ligament formation) as in original periodontium. Also, slow and/or improper repair of the PDL is associated with ankylosis between the roots unprotected by cementum and PDL and the corresponding alveolar bone (Wikesjo et al. 1988, J. Clin. Periodontol. 15:73-80). With current therapies, regeneration of soft tissue and bone in the healed wounds does not result in tissue with the anatomy, architecture, and thus function, characteristic of the original periodontium. In addition, none of the current therapies disclose predictable healing in periodontal disease of Class III furcation lesions which are "through-and-through", i.e. no bone in the lesion to begin with. (Pontoriero et al., 1989, J. Clin. Periodontol. 16:170-174).